27 - Chronic Kidney Disease Flashcards
What is done to identify chronic kidney disease in px w/ diabetes?
Screening for proteinuria & assessment of sCr converted into eGFR
All px w/ CKD considered high risk for _____
CV events
How can progression of CKD in diabetes be slowed?
Use of medications that disrupt RAAS
Earliest stage of diabetic nephropathy = ____
Hyperfiltration (GFR significantly higher than normal)
Earliest clinical sign of diabetic nephropathy is _____
Persistent albuminuria
What should be done for prevention of diabetic nephropathy?
- Optimal glycemic control ASAP after diagnosis will reduce risk of developing diabetic kidney disease
- Optimal BP control
- Blockade of RAAS w/ ACEi or ARB can reduce risk of developing CKD independent of their effect on BP (protective effect demonstrated in px w/ diabetes & HTN, but not normotensive px w/ diabetes)
What does albumin/creatinine ratio (ACR) describe?
- How much protein is in the urine and if there is renal dysfunction
- Need the ratio b/c don’t know if urine is dilute (drinking lots of water) or concentrated
- Creatinine shows how concentrated urine is
What do the values of ACR mean?
- ACR 2-20 = microalbuminuria
- ACR 20-66.7 = over nephropathy (macroalbuminuria)
What are some potential causes of transient albuminuria?
- Recent major exercise
- UTI
- Febrile illness
- Decompensated CHF
- Menstruation
- Acute severe elevation in blood glucose or BP
How can you decrease albuminuria?
Decrease amount of pressure on glomerulus
Which drug should be given to adults w/ diabetes & CKD w/ either HTN or albuminuria? What should be monitored?
- ACE inhibitor/ ARB and started at very low dose to slow progression of diabetic nephropathy
- Check sCr and K+ in first 2 weeks
- ACEi or ARB can cause dramatic increase in sCr in short period of time; this is caused by renal artery stenosis or on a sick day
- ACE inhibitor in type 1 w/ macroalbuminuria reduces renal outcomes
- Don’t use ACE & ARB together b/c increased risk of AKI & hyperkalemia
How long can ACEi or ARBs be safely continued in px w/ declining renal function over time?
Based on Lexicomp
- ACE inhibitors require dosage changes for renal dysfunction (decreased dose or frequency < 30 mL/min)
- ARBs don’t require dosage changes
What normally accompanies hyperphosphatemia?
Hypocalcemia and low serum levels of vitamin D
When are oral phosphate binders used?
Majority (over 90%) of px w/ kidney failure b/c dietary restriction isn’t enough to control hyperphosphatemia
Renagel - MOA, dose, SE, advantage, disadvantage
- Binds to phosphate w/o calcium (polysaccharide complex) so doesn’t cause hypercalcemia
- Usually 800 mg TID w/ meals
- GI effects (N/V, abdominal pain, bloating, diarrhea), hypercalcemia, metabolic acidosis
- Advantage = effective & doesn’t contain calcium & reduces LDL
- Disadvantage = GI effects & higher cost
Calcium carbonate - SE, advantage, disadvantage
- Interferes w/ absorption of aspirin, digoxin, isoniazid, quinolone, tetracycline
- AE = GI effects (N/V, diarrhea, constipation), hypercalcemia, xerostomia
- Advantage = effective & inexpensive
- Disadvantage = may contribute to hypercalcemia, promote vascular calcification, or both
What is the target phosphate serum level?
1.8 mmol/L
What is the relationship between the kidneys and vitamin D?
Kidneys are the final activation of vitamin D in the body, so when kidneys aren’t working then vitamin D doesn’t get activated
What is calcitriol?
- Activated vitamin D
- Has inhibitory effect on parathyroid gland
Which px can’t receive calcitriol?
Px w/ hypercalcemia (> 2.6) or hyperphosphatemia (> 1.8) b/c calcitriol will make phosphate & calcium higher (must control phosphates first)
What happens to phosphate in end stage renal disease?
Phosphate builds up in blood b/c can’t be filtered out by kidneys
What is the relationship between calcium and phosphate? Is this good?
Calcium & phosphate bind together, but don’t want calcium-phosphate to stay around in the body b/c will calcify in the arteries (called calcium phosphate deposition); also deposits in subcutaneous fat under skin (causes you to become very itchy; this can break the skin & cause infection)
Why don’t you want phosphate to be increased?
- Will bind to calcium and deposit in heart or subcutaneous fat
- Increased phosphate stimulates parathyroid gland (controls calcium levels) to release PTH (parathyroid hormone) that goes looking for calcium that needs to be replaced b/c phosphate is binding it all
- Will go to the bones to find the calcium => can lead to osteitis fibrosa cystica
How can phosphate be decreased?
Remove intake (processed meats, dairy products, can of soda)
Where do phosphate and calcium normally bind and where do we want them to bind?
- Normally phosphate & calcium bind in the blood
- Want it to happen in stomach so you can poop them out (that’s why you give calcium supplementation w/ meals)
What is the goal for PTH levels?
PTH (parathyroid hormone) should be < 200 ng/L in adults w/ chronic kidney disease (don’t know the exact amount for best protection)
What causes renal osteodystrophy? What is the tx?
- Caused by hyperphosphatemia b/c too much phosphate binds all the calcium, so body takes calcium from bones
- Tx would be treatment of high phosphate, which is phosphate binders (ex: Renagel)
